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D Y Graham

Publications and source records attributed to D Y Graham.

At least 217 records · Page 12Linked to original sources
PubMed1997

Furazolidone, amoxycillin, bismuth triple therapy for Helicobacter pylori infection.

BACKGROUND: Metronidazole-resistant Helicobacter pylori are generally the rule in developing countries such as Colombia. Developing countries need an effective, simple and inexpensive non-metronidazole therapy for H. pylori infection. AIM: To evaluate the combination of bismuth, furazolidone and amoxycillin for the treatment of H. pylori infection in Colombia. METHODS: Thirty patients with histologically documented H. pylori infection received the combination of bismuth subcitrate 240 mg b.d., furzolidone 100 mg q.d.s. and amoxycillin 500 mg q.d.s. for 14 days. Four or more weeks after ending therapy patients were re-endoscoped and gastric biopsies were obtained and examined using the Genta stain. Each slide was scored for presence, absence and density of H. pylori, active and chronic inflammation, intestinal metaplasia, erosions and atrophy. Cure was defined as the absence of H. pylori. RESULTS: All patients completed the course of therapy. Twenty-five patients were cured (86%, 95% CI: 65-94%). Mild, well-tolerated side-effects were reported by six patients (20%). CONCLUSIONS: This combination of bismuth, furazolidone and amoxycillin fulfills the criteria for successful H. pylori therapy and appears particularly well suited for developing countries since it is simple, inexpensive and effective. Furazolidone-containing therapies may become especially useful in the face of a world-wide increase in H. pylori resistance to metronidazole and macrolides.

Adult↗
PubMed1997

Successful low-dose amoxycillin, metronidazole and omeprazole combination therapy in a population with a high frequency of metronidazole-resistant Helicobacter pylori.

AIM: Effective anti-Helicobacter pylori therapies with few side-effects are needed. We studied the effectiveness of a low-dose combination of metronidazole, amoxycillin and omeprazole for treatment of ulcer patients in Seoul, Korea. METHODS: Patients with gastric or duodenal ulcer received metronidazole (125 mg b.d.), amoxycillin (500 mg b.d.) and omeprazole (20 mg at bedtime) for 2 weeks. Endoscopic examinations were performed before treatment and at least 6 weeks after completion of antimicrobial therapy. H. pylori status was confirmed by histological examination of two gastric biopsies using the Genta stain. RESULTS: Seventy-nine patients (64 men, 15 women, mean age 46 years) with peptic ulcer were enrolled. H. pylori infection was cured in 56 (71%) 95% CI: 60-81%). The cure rate in non-smokers was significantly higher than in smokers (88% vs. 65%, P = 0.035). Twelve pre-treatment isolates were available and metronidazole resistance was noted in all; H. pylori infection was cured in 10. Thirty-six patients cured of H. pylori have been followed for 1 year (mean of 361 days) and 2 cases became reinfected (5.5%, 95% CI: 1-18%). CONCLUSIONS: The low-dose combination of metronidazole, amoxycillin and omeprazole was effective even the in face of metronidazole resistance. Recurrence of H. pylori infection is infrequent even in countries with a high prevalence of H. pylori infection.

Adult↗
PubMed1997

Twice a day quadruple therapy (bismuth subsalicylate, tetracycline, metronidazole plus lansoprazole) for treatment of Helicobacter pylori infection.

BACKGROUND: Quadruple therapy (bismuth, metronidazole and tetracycline (BMT) + proton pump inhibitor) is touted as being > 95% effective, regardless of metronidazole resistance. We tested a 10-day b.d. quadruple therapy for treatment of H. pylori infection. METHODS: Anti-H. pylori therapy consisted of lansoprazole 15 mg b.d. plus tetracycline 500 mg b.d., metronidazole 500 mg b.d., and swallowable Pepto-Bismol caplets (2 b.d.) for 10 days. H. pylori status was evaluated by culture and histology before and 4 or more weeks after therapy. RESULTS: The cure rate for intention-to-treat was 70%. Treatment success was calculated overall and separately in relation to antimicrobial resistance patterns. The cure rate among the metronidazole-sensitive isolates was 89.7% (26 of 29) vs. 41.2% (7 of 17) of the metronidazole-resistant isolates (P < 0.005). Moderate (n = 1) or severe (n = 3) side-effects were experienced in four patients with only one withdrawing because of side-effects. CONCLUSION: Twice a day quadruple therapy is effective for metronidazole-sensitive strains but its usefulness is markedly reduced by the presence of pre-treatment metronidazole resistance. Twice a day quadruple therapy can be recommended in locations where background metronidazole resistance is uncommon. Possibly, 14-day therapy or a higher dosage of metronidazole provide better results with metronidazole-resistant H. pylori.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1997

Clarithromycin, amoxycillin and H2-receptor antagonist therapy for Helicobacter pylori peptic ulcer disease in Korea.

BACKGROUND: Effective anti-Helicobacter pylori therapies with few side-effects are needed. We previously showed that the regimen of amoxycillin, clarithromycin and an H2-receptor antagonist was effective in the United States. The current study tested whether this therapy would also be successful in Korea. METHODS: Patients with gastric or duodenal ulcers received amoxycillin (750 mg t.d.s.) plus clarithromycin (500 mg t.d.s.) for 2 weeks and nizatidine 300 mg at bedtime for 6 weeks. Endoscopic examinations were performed before treatment and 4 or more weeks after ending antimicrobial therapy. H. pylori status was confirmed by rapid urease testing and histological examination of gastric antrum and corpus biopsies using the Genta stain. Antibiotic resistance was tested using the E-test method. Cure was defined as no evidence of H. pylori infection 4 or more weeks after ending therapy. RESULTS: Seventy-two patients (59 males and 13 females; mean age 46 years), including 35 with duodenal ulcers, 30 with gastric ulcers and seven with both, were studied. H. pylori infection was cured in 95.8% (69/72 patients; 95% CI = 88.3-99.1%). Two of the treatment failures had culture data and one had pre-treatment resistance to clarithromycin. Smoking did not have an adverse effect on therapy. Ten patients (15%) developed side-effects during treatment, but all were mild and did not require treatment interruption. No case of reinfection was noted during follow-up. CONCLUSION: The combination of amoxycillin, clarithromycin and an H2-receptor antagonist is effective in Korean patients with H. pylori infection.

Adolescent↗
PubMed1997

Lack of dose-response with Pancrease MT for the treatment of exocrine pancreatic insufficiency in adults.

BACKGROUND: Choosing the optimum pancreatic enzyme replacement therapy for patients with exocrine insufficiency remains a problem. An enteric coated enzyme microsphere pancreatic enzyme preparation (Pancrease) has been marketed with several levels of lipase activity, implying that there is a dose-response relationship between dose and effectiveness such that the high potency form appears to be the most cost effective. METHODS: In a randomized, single-blind, cross-over study, we evaluated the effectiveness of a commercial enzyme preparation with different amounts of lipase per dosage unit in adults with exocrine pancreatic insufficiency. Patients received a diet comprising 100 g fat each day for 6 days. With each meal (three per day) they received two capsules of either Pancrease MT4 (8000 unit lipase), Pancrease MT10 (20,000 units lipase), Pancrease MT16 (32,000 units lipase) or placebo. A 72-h quantitative faecal collection was carried out for the last 3 days of the 6-day period. RESULTS: There was a reduction in faecal fat excretion with each of the preparations compared to placebo. The difference failed to reach significance with the 8000 units lipase preparation (P > 0.05) but was significant (P = 0.02) with the 20,000 units lipase and the 32,000 units lipase preparations (faecal fat excretion: placebo = 42.1 +/- 29 g, lipase 8000 = 22.1 +/- 7.3 g, lipase 20,000 = 10.2 +/- 4.5 g and lipase 32,000 = 15.8 +/- 12.5 g, P < for 20,000 units and 32,000 units lipase compared to placebo). CONCLUSION: A dose-response relationship between the amount of lipase administered with each meal and a reduction in faecal fat was not evident. The most potent preparation did not provide additional benefits compared to the less expensive lower potency dosage form.

Adult↗
PubMed1997

Point mutations in the 23S rRNA gene of Helicobacter pylori associated with different levels of clarithromycin resistance.

Fifty-four of 59 (91.5%) clarithromycin-resistant isolates of Helicobacter pylori from different patients possessed either the A2143G (formerly A2058G) or the A2144G (formerly A2059G) mutation in the gene encoding 23S rRNA. The A2143G mutation was significantly more likely to occur in isolates with MICs exceeding 64 mg/L (65% versus 30% with the A2144G mutation; P = 0.01). The majority (26 of 31; 83.9%) of isolates with the A2143G mutation had MICs exceeding 64 mg/L. Peptic ulcer disease recurred in a substantial proportion of patients infected with H. pylori strains containing either the A2143G or the A2144G mutation.

Anti-Bacterial Agents↗
PubMed1997

Failure to isolate Helicobacter pylori from stray cats indicates that H. pylori in cats may be an anthroponosis--an animal infection with a human pathogen.

The recent isolation of Helicobacter pylori from cats obtained from a commercial supplier has potentially important public health implications. The present study investigated whether H. pylori infection was common in stray cats. Twenty-five cats were examined for the presence of H. pylori by histological examination, culture and two polymerase chain reaction (PCR) assays. Histologically, the gastric biopsy specimens from all cats showed large spiral organisms typical of H. felis and not H. pylori. Samples from 23 cats yielded bacterial growth and two had no growth. Colonies grossly similar to H. pylori were tested for catalase, oxidase, urease and Gram's stain reactions. None was H. pylori. All samples tested as positive by the Helicobacter 16S rRNA genus-specific PCR assay and only six cats and a mouse stomach infected with H. heilmannii gave positive results with the adhesin subunit A (hpaA)-specific PCR assay, which is consistent with either H. pylori or H. heilmannii. The helicobacters identified in these samples by PCR were not cultivable and hence were probably H. heilmannii. H. pylori infection is uncommon in stray cats and owning pet cats should not be a threat to public health in relation to H. pylori infection.

Adhesins, Bacterial↗
PubMed1997

Perturbations in gastric physiology in Helicobacter pylori duodenal ulcer: are they all epiphenomena?

BACKGROUND: The Holy Grail of physiological studies in acid secretion has been to identify a specific abnormality in gastroduodenal physiology responsible for the development of duodenal ulcer disease. METHODS: We review the available data relating duodenal ulcer and Helicobacter pylori infection to perturbations in gastric physiology, especially acid secretion. RESULTS: It is known now that elevated serum pepsinogen levels, reduced inhibition of acid secretion with antral acidification or distention, exaggerated gastrin response to meals or infusion of bombesin or gastric-releasing peptide, exaggerated acid output in response to gastric-releasing peptide, and abnormalities in duodenal bicarbonate secretion in response to instillation of acid are reversible epiphenomena related to the H. pylori infection and are not in themselves responsible for duodenal ulcer disease. H. pylori is inhibited by bile, yet can thrive in the duodenal bulb of duodenal ulcer patients. Glycine-conjugated bile acids are precipitated by acid; thus, any mechanism that would increase the duodenal acid load may remove the inhibitory bile and allow unrestrained growth of H. pylori. CONCLUSION: These data and speculations offer one possible explanation for why duodenal ulcer occurs in only some people--those with high acid secretion--and suggest that the combination of high duodenal acid load and H. pylori infection is sufficient to result in duodenal ulcer disease.

Duodenal Ulcer↗
PubMed1997

Primary gastric MALT lymphoma: trivial condition or serious disease?

BACKGROUND: Primary gastric B-cell lymphomas originating from the mucosa-associated lymphoid tissue (MALT) have been demonstrated to be closely associated with Helicobacter pylori infection. Approximately 70% of these tumors regress within 1 year of eradication of H. pylori. Currently, there is little consensus on the best strategies for diagnosing, treating, and following up these lymphomas. Our objective was to review the current strategies for the diagnosis and management of MALT lymphomas and to describe the management guidelines used in our own institution. METHODS: Our approach consisted of a review of the literature and personal experience. RESULTS: Rigorous histopathological criteria (Isaacson's criteria) must be applied to the diagnosis of gastric biopsies with atypical lymphoid aggregates. Molecular and immunohistochemical studies might play have a role in determining the clonality of the lesions, but correlation with the histopathological aspects is crucial. CONCLUSIONS: Little solid information exists on the natural history and evolution of MALT lymphomas. While studies are being carried out, we suggest that even a suspected MALT lymphoma in a gastric biopsy specimen should be treated as a potentially serious condition. The diagnosis should be confirmed by an experienced histopathological laboratory, and H. pylori infection must be sought and treated. Because the response of lymphomas to antibacterial therapy cannot be predicted, close follow-up of affected patients is essential.

Helicobacter Infections↗
PubMed1997

Effects of smoking on cure of Helicobacter pylori infection and duodenal ulcer recurrence in patients treated with clarithromycin and omeprazole.

BACKGROUND: Smoking may affect adversely the cure rate for Helicobacter pylori infection in patients treated with amoxicillin and omeprazole. Therapy with clarithromycin and omeprazole was tested for its effectiveness in the treatment of H. pylori infection in smokers and nonsmokers. MATERIALS AND METHODS: Patients with verified duodenal ulcer and H. pylori infection received clarithromycin 500 mg tid, in combination with omeprazole 40 mg/ day, for 2 weeks, followed by omeprazole (20 or 40 mg daily) for 2 additional weeks according to a randomized, double-blind, multicenter design. Patients were analyzed by their smoking status for the cure of H. pylori infection, ulcer healing, and prevention of duodenal ulcer recurrence. RESULTS: After treatment with clarithromycin and omeprazole, H. pylori infection was cured in 71% of the smokers and in 77% of the nonsmokers (evaluated 4-6 weeks after treatment). Overall ulcer healing was 95%, and overall ulcer recurrence was 19%. For H. pylori-negative patients, ulcer recurrence was 12% in both smokers and nonsmokers. None of these values was significantly different when smokers were compared to nonsmokers. CONCLUSIONS: Therapy with clarithromycin and omeprazole is effective for cure of H. pylori infection in smokers and nonsmokers. Smoking has no effect on duodenal ulcer healing or duodenal ulcer recurrence for patients treated with this regimen.

Adult↗
PubMed1997

Invasive Helicobacter-like organisms in feline gastric mucosa.

BACKGROUND: Helicobacter-like organisms (HLOs) usually are present in the stomachs of cats. Although the histopathology of natural (H. felis or H. heilmannii) infections has been reported, their invasion into the lymphoid aggregates has not been described previously. MATERIALS AND METHODS: Gastric tissues were obtained from 17 adult cats living in a natural urban environment. Biopsy sites were selected by the presence of urease on the mucosal surface stained by Genta stain and periodic acid-Schiff stain. RESULTS: Spiral organisms morphologically similar to H. felis or to H. heilmannii were detected in all the cats, distributed predominantly over the oxyntic mucosa. Seven cats had prominent lymphoid follicles with germinal centers within the oxyntic mucosa, and in six of these seven cats, extracellular organisms were present within the lymphoid follicles. Scattered organisms also were found over sites of gastric metaplasia in the duodenum of six cats. CONCLUSIONS: This study extends previous observations by showing that HLO infection in cats is associated with large lymphoid follicles in the stomach. In addition, HLOs were demonstrated submucosally within gastric lymphoid follicles and on patches of gastric metaplasia in the duodenum.

Animals↗
PubMed1997

Decrease in gastric permeability to sucrose following cure of Helicobacter pylori infection.

BACKGROUND: Gastric sucrose permeability is a noninvasive marker that reliably increases in association with gastrointestinal injury due to use of nonsteroidal antiinflammatory drugs. Despite the effect of Helicobacter pylori infection on the gastric mucosa, in a previous study we were unable to demonstrate that H. pylori infection was associated with abnormal gastric sucrose permeability. Our goal in this study was to explore further whether H. pylori infection changed gastric permeability; therefore, we evaluated the effect of treatment of H. pylori infection on gastric permeability to sucrose and the relation of sucrose permeability to density of polymorphonuclear leukocytes. MATERIALS AND METHODS: Five hundred milliliters of a solution containing 100 gm of sucrose was ingested by the subject at bedtime. Overnight urine was collected and assayed for sucrose by high-performance liquid chromatography. Sucrose permeability was assessed both before and approximately 4 weeks after anti-H. pylori therapy. RESULTS: Seventeen asymptomatic H. pylori-infected volunteers participated; 8 were cured. Sucrose permeability was in the range commonly found in normal controls both before and after anti-H. pylori therapy (mean excretion, 76.3 mg; range, 13-171 mg). Gastric sucrose permeability correlated with the density of polymorphonulcear cell infiltration of the mucosa. Cure of the H. pylori infection was associated with a small but significant decrease in sucrose permeability (98.8 +/- 18 mg to 51.7 +/- 9.8 mg (p = .01). Sucrose permeability was greater in those with a high density of mucosal polymorphonuclear cells compared to those with lower scores (119.5 +/- 4 vs 71.4 +/- 13 for those with scores > or = 5 compared to scores < or = 4; p = .023). Failed therapy resulted in an increase in the mucosal density of polymorphonuclear infiltration and sucrose permeability (56.4 +/- 13 mg-99.7 +/- 19 mg pretreatment vs posttreatment, respectively; p = .031). CONCLUSION: H. pylori gastritis causes a small but measurable increase in gastric permeability to sucrose that may reflect epithelial transmigration of neutrophils.

Anti-Bacterial Agents↗
PubMed1997

Development of a murine model of Helicobacter pylori infection.

BACKGROUND: A murine model for Helicobacter pylori infection could facilitate vaccine development. This study was designed to determine the effect of various conditions of dose, frequency of administration, and fasting on H. pylori infection of mice. MATERIALS AND METHODS: Balb/c and C3H/HeN mice were inoculated orogastrically with clinical isolates of H. pylori grown in liquid culture. At 2-week intervals, the stomachs were removed for secondary culture on horse blood agar and for histological analysis. H. pylori from secondary cultures or homogenized stomach tissue from infected mice was inoculated a second time in naïve animals. RESULTS: H. pylori was cultured with high frequency only from the stomachs of C3H/HeN mice. Fasting the mice and increasing the number of organisms inoculated did not increase the rate of infection. Histological analysis detected no inflammation, but mucus depletion and erosion were present in the stomachs of C3H/HeN mice. H. pylori organisms were not observed. Secondary cultures of H. pylori or homogenized infected stomach tissue did not cause infection when inoculated in naïve mice. CONCLUSIONS: Clinical isolates of H. pylori transiently infect C3H/HeN mice. This murine model is suitable for testing oral vaccines. Effective vaccination against H. pylori could prevent transient infection and reduce subsequent gastritis.

Animals↗
PubMed1997

Co-existing gastric cancer and duodenal ulcer disease: role of Helicobacter pylori infection.

BACKGROUND: The association of gastric cancer and chronic duodenal ulcer disease is considered rare. In fact duodenal ulcer disease is believed to somehow "protect" against the development of gastric cancer. Helicobacter pylori infection is an important factor in the development of gastric cancer. No detailed investigation on the prevalence of H. pylori in coexistence of gastric cancer and duodenal ulcer disease has been performed. We evaluated the frequency of H. pylori infection in the patients with co-existence of gastric cancer and duodenal ulcer disease. MATERIALS AND METHODS: During the period March 1994 to February 1995, we collected data from 3,652 patients in whom esophagogastroduodenoscopy was done. During this period, when the cancerous or ulcerative lesions in stomach or duodenum were found, rapid urease tests were performed. RESULTS: Six patients had concurrent gastric carcinoma and duodenal ulcer disease. Three of the cases had early gastric carcinoma; 2 had active duodenal ulcers and one had a duodenal ulcer scar; all 3 had positive rapid urease tests. The patients with early gastric cancer were younger than the individuals with advanced gastric cancer. CONCLUSIONS: The co-existence of both diseases may be higher than reported from Western countries or from Peru which may either reflect the high prevalence of circulation of H. pylori ulcer and cancer strains in Korea and the co-infection with both types of organism in some individuals.

Adult↗
PubMed1997

A PCR-oligonucleotide ligation assay to determine the prevalence of 23S rRNA gene mutations in clarithromycin-resistant Helicobacter pylori.

We have developed a rapid PCR-oligonucleotide ligation assay that can discriminate single base substitutions that are associated with clarithromycin resistance in Helicobacter pylori. Susceptible isolates were wild type at positions 2143 and 2144 (cognate to 2058 and 2059 in Escherichia coli), while 93% of the resistant isolates contained A-to-G mutations at either position and 7% of the isolates contained A-to-C mutations at position 2143. In addition, the MIC for 86% of the resistant isolates with an A2143 mutation was > or = 64 micrograms per ml, and that for 89% of the resistant isolates with an A2144 mutation was < or = 32 micrograms per ml.

Anti-Bacterial Agents↗
PubMed1997

Differential stimulation of interleukin-12 (IL-12) and IL-10 by live and killed Helicobacter pylori in vitro and association of IL-12 production with gamma interferon-producing T cells in the human gastric mucosa.

The objective of these experiments was to examine the ability of Helicobacter pylori to stimulate interleukin-10 (IL-10) or IL-12 and select for either Th1 or Th2 cells. Gastric biopsy specimens were collected from patients who were categorized with respect to the presence of H. pylori and gastric disease as well as their age, gender, medications, and other factors. As Th1 and Th2 cells are selected by IL-12 and IL-10, respectively, biopsy specimens were screened for mRNA and protein for these cytokines. Although mRNA for IL-12 and IL-10 was detected in biopsy specimens obtained from both infected and uninfected patients, IL-12 protein predominated. Levels of IL-10 and IL-12 in gastric tissue did not change in response to infection. Moreover, gamma interferon (IFN-gamma)-producing T cells were found in both the infected and the uninfected gastric mucosa. Stimulation of peripheral blood leukocytes from either infected or uninfected donors with various concentrations of live or killed H. pylori induced immunoreactive IL-12 and IL-10. After stimulation with live H. pylori, IL-12 levels increased more than 30-fold, whereas IL-10 levels increased only 2- to 5-fold, compared to cells stimulated with medium alone. Interestingly, killed H. pylori induced significantly more IL-10 (P < 0.05) than live H. pylori, while recombinant urease only induced IL-10. These results demonstrate that live H. pylori selectively stimulates the induction of IL-12 and Th1 cells that produce IFN-gamma, whereas preparations used in oral vaccines induce more IL-10 and may favor Th2 cell responses.

Adult↗
PubMed1997

Characterization of a specific Mycobacterium paratuberculosis recombinant clone expressing 35,000-molecular-weight antigen and reactivity with sera from animals with clinical and subclinical Johne's disease.

Johne's disease is a chronic enteritis of ruminants associated with enormous worldwide economic losses for the dairy cow- and goat-rearing industries. Management limitations and eradication programs for this disease have been hampered by the lack of a simple and specific diagnostic test for the detection of subclinical cases. We used a recombinant clone expressing a 35,000-molecular-weight Mycobacterium paratuberculosis antigen (p35 antigen) from a previously constructed expression library of M. paratuberculosis in Escherichia coli. The DNA fragment encoding the p35 gene hybridized only to DNA from Mycobacterium avium complex, but not to DNAs from other mycobacteria and nonmycobacterial organisms. The seroreactivity of p35 was evaluated by immunoblotting against 57 reference serum samples obtained from infected and uninfected animals. p35 was recognized by sera from 100% of animals with advanced Johne's disease (clinical stage) (12 cattle, 2 goats, and 2 sheep) and by sera from 75% of 20 cattle with early infection (subclinical stage). None of the sera from 15 M. paratuberculosis-free cows, 3 Mycobacterium bovis BCG-infected tuberculous cattle, or 3 cows artificially inoculated with multiple doses of viable M. paratuberculosis reacted with p35. The overall sensitivity, specificity, positive predictive value, and negative predictive value were 86, 100, 100, and 75%, respectively. The accuracy of p35 immunoblotting was superior to those of commercially available diagnostic tests for Johne's disease. These results suggest that the p35 recombinant protein has potential for use in the serodiagnosis of animals with Johne's disease at all stages of infection. The DNA fragment encoding p35 may also serve as a probe for identification of M. avium complex infection.

Animals↗